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September lectures yr 3 (2018) > Biochemical aspects of GI disease and nutrition > Flashcards

Biochemical aspects of GI disease and nutrition Flashcards

1
Q

During a clinical assessment what is normal for the patient in terms of nutrition?

A

weight - loss or gain (intentional or unintentional)
food intake
chewing/swallowing
GI symptoms - nausea, vomiting, altered bowel habits
drugs/alcohol

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2
Q

How can you assess food intake?

A

dietary recall
food diaries - unweighed food record
food weighing

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3
Q

What functional assessments can be done to assess nutritional status?

A

muscle mass - grip strength / isometric knee extension / response to electrical stimulation

hepatic secretory proteins - albumin (<35) and transferrin (<1.5g/L)

immune response in malnourished patients - cell mediated immunity

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4
Q

How is malabsorption defined?

A

wide group of conditions associated with disordered biochemistry
no specific clinical presentation - may be a group of signs or symptoms

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5
Q

What is the prevalence of undernutrition in hospital?

A

40%

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6
Q

What are the effects of malnutrition?

A

Impaired immune response - infection
decreased respiratory muscle strength - increased incidence of chest infection
impaired wound healing - prolonged recovery
inactivity - thromboembolism, pressure sores
decreased skeletal muscle strength - fatigue, inactivity, falls
impaired thermoregulation - hypothermia

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7
Q

How does malabsorption present and why?

A 
pale bulky (offensive) stools  - fat malabsorption or digestion 
abdominal distention, watery diarrhoea, and xs flatus - malabsorption of carbohydrate 
vague malaise, tiredness and weight loss - generalised deficiency of nutrients 
anaemia - deficiency of iron folate or B12 
easy bruising or bleeding  - deficiency of vit K 
failure to thrive - generalised deficiency of nutrients
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8
Q

How can you estimate nutritional requirements?

A

energy requirements = calorimetry
estimation from body weight = 25-35 kcal/kg/24 hours
prediction equations = schofield equation, harris-benedict equation and ireton-jones formula

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9
Q

How is basal metabolic rate calculated?

A

Male
BMR = 66.5 +13.75Weight +(5height-6.77age)

Female
BMR = 66.5 +19.56Weight +(1.85height-4.67age)

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10
Q

How does BMR vary between age and height?

A

With increasing height your BMR increases and with increasing age your BMR reduces

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11
Q

What are the different types of sugars?

A

intrinsic = naturally e.g. as part of the cellular structure

extrinsic = non-natural e.g. refined sugars

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12
Q

What are the different types of starches?

A

alpha glucan polysaccharides
Amylose= straight chain glucose polymer with molecular mass 100,000Da
Amylopectin = branched chain glucose polymer with molecular mass >100,000

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13
Q

How are carbohydrates chemically digested?

A

salivary amylase, pancreatic amylase and brush border enzymes (dextrinase, glucoamylase, lactase, maltase and sucrase)

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14
Q

How are carbohydrates absorbed?

A

secondary active transport (cotransport) with Na
Facilitated diffusion of some monosaccharides = enter the capillary beds in the villi, transported to the liver via the hepatic portal vein

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15
Q

Where is amylase found and what does it produce?

A

salivary and pancreatic
- digestion of alpha1,4- bonds in starch
= produces = maltose, maltotriose, short branched oligosaccharides and alpha-limit dextrins

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16
Q

How does maltase work and what does it produce?

A

splits glucose from alpha-1,4 bonds in starch up to 9 residues long
producing glucose

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17
Q

How does sucrase work and what does it produce?

A

splits sucrose producing glucose and fructose

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18
Q

How does isomaltase work and what does it produce?

A

splits glucose monomers from non-reducing ends of alpha limit dextrins
producing glucose

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19
Q

How does lactase work and what does it produce?

A

splits lactose producing galactose and glucose

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20
Q

How much of dietary starch isn’t absorbed?

A

up to 20%
- carbohydrates in the bowel are metabolised by bacteria to produce short chain fatty acids (energy source for colonocytes) + methane + hydrogen

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21
Q

What are primary and secondary lactase deficiencies?

A

primary = eu 5-15%, africans/asians >70%

secondary = IBD, chronic alcoholism, coeliac disease, tropical sprue

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22
Q

How can you investigate for carbohydrate absorption?

A

xylose absorption
- pentose sugar 50% excreted in urine - not reliable test so not used

lactose intolerance test
- serial glucose measurements after 50g lactose

hydrogen breath tests

  • glucose hydrogen breath test = bacterial overgrowth in the small intestine
  • lactose hydrogen breath test = problem digesting lactose
  • fructose hydrogen breath test = difficulty digesting fructose
  • sorbitol hydrogen breath test = sorbitol is a sugar alcohol used to to investigate rapid intestinal transit
  • lactulose hydrogen breath test = galactose and fructose transported intact to the colon measure of ororectal transit time
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23
Q

How is fat absorbed?

A

emulsified by bile phospholipids
stabilised by bile salts
lipase digestion to monoacylglycerol and free fatty acids
solubilised in micelles

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24
Q

What are the stages of fat digestion and absorption?

A

1) pre-treatment = emulsification by bile salts
2) enzymes - pancreatic lipase
3) absorption of glycerol and short chain fatty acids = absorbed into capillary blood villi and transported via hepatic portal vein

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25
How are monoglycerides and fatty acids absorbed?
cluster with bile salts and lecithin to form micelles then released by micelles to diffuse into epithelial cells then combine with proteins to form chylomicrons then enter lacteals and are transported to systemic circulation
26
What are essential fatty acids?
phospholipids - linoleic acid and alpha- linoleic acid precursors of arachadonic acid, eicosapenaenoic acid and docosahexaenoic acid
27
What is fat absorption dependent upon?
bile production - dependent on liver secretion = bile salts, phospholipids and cholesterol and also having patent ducts pancreatic enzymes = functional lipase
28
How can fat absorption be investigated?
faecal fat excretion - 3/5 day collection - usual diet pre-collection - outmoded, no longer used 14C-triolein breath test - if 14C labelled triolein absorbed, 14C02 will appear in breath - but lung/liver disease may give false results
29
How are proteins digested and absorbed?
pepsin in stomach pancreatic proteases = trypsin, chymotrypsin and carboxypeptidase brush border enzymes = aminopeptidases, carboxypeptidases and dipeptidases absorption of amino acids is coupled to active transport of Na
30
How can protein metabolism be measured?
nitrogen balance - pts on ITU or long term nutrition - nitrogen excretion = urinary nitrogen + faecal nitrogen - variability of faecal output
31
What is urinary nitrogen made up of?
urinary urea nitrogen and non-urea nitrogen (20%) - urinary urea nitrogen can be used as an assessment tool but is less useful with increasing severity of illness and inaccurate where there is urine infection
32
What is faecal pancreatic elastase 1?
elastase is a protein cleaving enzyme produced by the pancreas resistant to degradation by other enzymes and is excreted into the gut therefore it can be measured in the stool - enzyme is reduced in pancreatic insufficiency
33
What is serum immunoreactive trypsin (IRT)?
assessing pancreatic function - increased IRT indicates obstruction - used as a screening test for CF in new born babies - low serum values indicate failure of production in pancreatic disease
34
Where are vitamins absorbed?
small intestine - fat soluble = A, D, E and K - carried by micelles and then diffuse into absorptive cells - water soluble vitamins= B and C are absorbed by diffusion or by passive or active transporters - vit b12 binds to intrinsic factor and is absorbed by endocytosis
35
What vitamins are absorbed in the large intestine?
K and B from bacterial metabolism
36
What are some sources of vitamin A ?
preformed vit A = retinol - liver, fish oils, diary Carotenoid pigments - beta-carotene - carrots, dark green leafy veg
37
What happens if you have vit A deficiency?
night blindness
38
What happens if you have an excess of vit A?
Acute - raised ICP, nausea, vomiting, visual disturbances chronic - liver/bone damage+/- teratogeneicity
39
What are the sources of vit E?
8 similar compounds - intake is proportional to intake of polyunsaturated fatty acids - tocopherols = alpha is the most abundant present in cell membranes - antioxidant
40
What happens if you have a deficiency of vit E?
premature infants= haemolytic anaemia and thrombocytopenia Children/young adults spinocerebellar degeneration parenteral nutrition
41
What happens if you have an excess of vit E?
relatively non-toxic
42
What are sources of thiamine / vitamin B1?
wheat germ, oatmeal and yeast
43
What happens if you are deficient in thiamine?
beriberi - dry = peripheral neuropathy, muscle weakness, fatigue - wet = oedema and heart failure common in 1st world as wernickes encephalopathy
44
How is a thiamine deficiency assessment carried out?
direct measurement of thiamine before giving any | - previously erythrocyte transketolase measurement - not used for assessment
45
What happens if you have an excess of thiamine?
non- toxic | not recognised as a problem
46
What are some sources of riboflavin / vitamin B2?
flavoproteins = flavin mononucleotide, flavin adenine dinucleotide = electron carrier in biological oxido-reduction systems sources = eggs, green veg, milk and meat
47
What happens if you have a deficiency of riboflavin?
angular stomatitis, painful red tongue with sore throat oily scaly skin rashes eye sensitive to light anaemia birth defects including congenital heart defects and limb deformities
48
How is a riboflavin deficiency assessed?
``` urinary excretion (poor measure) red cell glutathione reductase (very limited use) ```
49
What are some sources of nicotinamide/vitamin B3?
yeast, meat, milk and green veg
50
What does a deficiency in nicotinamide/b3 cause?
pellagra = rare in developed world usually secondary to alcoholism, long term diarrhoea replacement is non-toxic
51
What are some sources of vitamin B6?
pyridoxal, pyridoxine, pyridoxamine + 5-phosphates = fortified breakfast cereals, meat, bananas, chickpeas, potatoes, pistachios
52
What does a deficiency in vitamin B6 cause?
seborrhoeic dermaitis, atrophic glossitis, neurologic symptoms of somnolence, confusion, neuropathy and sideroblastic anaemia
53
What is zinc an essential component of and what does a deficiency cause?
essential for over 200 enzymes | - deficiency = inadequate intake (parenteral feeding) and increased loss (diarrhoea)
54
How can you assess zinc levels?
plasma zinc urinary zinc used in pts on parenteral nutrition
55
What can an excess of copper cause?
difficult to cause an excess Wilson's disease - assess by looking at plasma and urine copper and caeruloplasmin
56
What is selenium important for and what happens with deficiency and excess?
essential co-factor of glutathione peroxidase deficiency = parental nutrition excess - animals, poisoning
57
What are the key ways of supplementing nutrition?
food supplements enteral (using gut) parenteral (using IV)
58
What is enteral feeding?
``` nutrients delivered to the gut - stimulate gut hormones - helps maintain gut integrity - nutrients absorbed into portal circulation - more physiological than TPN there are different routes of delivery ```
59
What are the indications for enteral nutrition?
disturbed swallowing e.g.MND upper GI obstruction e.f. oesophageal stricture Inability to eat e.g. head injury, critical illness GI disease e.g. pancreatic insufficiency High requirements e.g. burns, trauma Loss of appetite e.g. anorexia nervosa, cardiac cachexia
60
What are the sources of delivery of enteral feeds?
into the stomach - nasogastric or orogastric tube - gastrostomy - oesophagostomy beyond stomach - nasoduodenal tube - jejunostomy
61
How does TPN work?
via circulation therefore bypassess GIT and liver (1st pass metabolism) 3 chamber inner bag - glucose, amino acids and fat emulsion separately - oxygen absorber and then overpouch (light sensitive) - intralipid can cause fever, shivering, chills and N+V but rare
62
What are the indications for TPN?
Lack of functioning GIT "intestinal failure" - blockage - reduced absorptive capability - temporary or permanent the oral/enteral route will not maintain adequate nutrition - eg. premature infant needs to rest GIT - gastroschisis prolonged diarrhoea - high output fistulae - anastomosis
63
What are some causes of hypokalaemia?
insufficient for excessive losses/depletion | e.g. D+V, renal or anabolic phase i.e. refeeding, insulin or alkalosis
64
What are some causes of hyperkalaemia?
renal failure, increase catabolism and cell breakdown, acidosis
65
What are the causes of hyponatraemia?
pseudo due to lipaemia increased ADH release and poor regulation of fluid balance water overload/ Na loss rarely high loss e.g. fistula, drain, renal need low Na and H20 feed if hypo seconadry to ascites / oedema
66
What are some causes of metabolic bone disease?
steroid use, SBS, inactivity, menopause
67
What is refeeding syndrome?
consisting of metabolic disturbances that occur as a result of reinstitution of nutrition to patients who are starved, severly malnourished or metabolically stressed due to severe illness when too much food and/or liquid nutrition supplement is consumed during initial 4-7 days of re-feeding => synthesis of glycogen, fat and protein in cells, to the detriment of serum conc of K, Mg and phosphorus the low serum minerals, if severe enough can be fatal
68
What patients are at risk of re-feeding syndrome?
``` pts with anorexia nervosa pts with chronic alcoholism oncology pts postoperative pts elderly patients uncontrolled DM chronic malnutrition long term use of antacids long term use of diuretics ```
69
What is calprotectin a sign for ?
used to investigate the cause persistent watery or blood diarrhoea can be requested with stool culture to detect bacterial infection -useful to determine if IBD or IBS
70
What is faecal immunohistochemical test?
type of faecal occult blood test - uses antibodies that specifically recognise human hb - used to detect and quantify the amount of blood in a single stool sample

September lectures yr 3 (2018) (56 decks)

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